Activity dependent plasticity Flashcards
how many layers does the neocortex have
6 layers
what is layer IV
thalamo-recipient layer
prey vs predator visual anatomy
prey = eyes on side
predator = eyes on the front
visual system route
retina
LGN
striate cortex (IV)
what stains retinotopic maps
cytochrome oxidase
what does optical imaging measure for
amount of oxygenated blood (activity)
Sur, Garraghty & Roe (1988)
Turning auditory cortex into visual cortex (Ferret)
lesion collicular pathway
loss of auditory input to MGN
feed optic nerve into LGN and MGN
develops orientation specific neurons in A1 which respond to visual features
what is hebbian plasticity
modification of existing connections between neurons
criteria to implement hebbian plasticity
activity dependence between pre and post synaptic neurons
input specificity (inputs co-active with post synaptic cells)
cooperativity (multiple inputs at once)
associativity (info from 2 sources can be integrated)
longevity (change should last for a specific period)
long term potentiation LTP
artificial hebbian plasticity
tetanus (100Hz) causes LTP
(beck at el., 2000)
Input specificity of LTP
Insert 2 electrodes in human hippocampal slice (DG)
Input 1 - baseline and tetanus causes LTP after high frequency stimulation
Input 2 - baseline only
AMPA receptor
ionotropic glutamate receptor which allows Na+ ion influx via electrostatic and diffusion movement
AMPA R antagonist
CNQX
NMDA receptor
coincidence detector/induction mechanism
It is ligand and voltage gated
Blockade via Mg2+ in pore
depolarisation removes Mg2+ blockade
NMDAR antagonist (AP5/APV) blocks LTP induction
LTD features
LTD is input specific and dependent on NMDAR like LTP
(fire out of sync lose your link)
HFS/LFS of the post synaptic cell
HFS - temporal summation - high 5um Ca2+ - protein kinases increase AMPAR function
LFS - low 1um Ca2+ - protein phosphatase decrease AMPAR function
overstimulation can cause epilepsy/coma
ocular dominance
contralateral and ipsilateral inputs segregated in L4 (binocular vision requires C&I integration)
ocular dominance occurs in L4 of primate/striate cortex
autoradiography tracks ocular dominance (retina-LGN-striate cortex)
methods to inactivate the retina
Colombian tree frog (epibatidine)
newts and pufferfish/fugu - tetrodotoxin TTX - blocks VGSC
Huberman et al., 2003 - normal eye opening occurs at p1-10 in ferret - segregation occurs in LGN, epibatidine inactivates the retina and causes blurred segregation
spontaneous activity not correlated between the two retina
what is needed for segregation zones in mouse SI
Iwasato et al., 2000
NMDAR
CXNR1 KO causes no whisker barrel formation
Hubel & Wiesel
monocular deprivation in kittens
monocular deprivation of contralateral eye - open contralateral eye - almost all neurons responsive to ipsilateral eye
strabismus (squint) of contralateral eye - equal distribution of responsive neurons
monocular deprivation of contralateral eye - open contralateral eye and NMDAR blockade - no OD shift
therefore, monocular deprivation causes a shift in organisation in LGN & L4 of V1, LTD like plasticity (use it or lose it)
ganglion cell receptive field
centre - positive maximal activity
surround - negative minimal activity
ganglion cells differ in firing APs
orientation selectivity
orientation selectivity to experience dependence (Ca2+ dependence) - blocked by NMDAR antagonist APV
feedforward excitation from LGN relay cells and summate to form orientation selectivity and intracortical lateral inhibition
critical period
monocular deprivation in cats
5wks (OD shift is reversible in kittens) - monocular deprivation of the contralateral eye and reverse suture - close ipsilateral eye- recovers binocular dominance in contralateral eye
14wks - no plasticity (critical period is closed) recently closed ipsilateral eye is dominant
cortical inhibition and the critical period
low cortical inhibition - no plasticity
high cortical inhibition - critical period closes
feedforward GABA inhibition is needed to open the critical period
little inhibition = improper coding = no OD plasticity (hence no critical period)
Human Amblyopia
lazy eye - cortical blindness
reduced visual acuity in otherwise healthy and properly corrected eye
no depth perception- prevents employment
2% of UK population is affected
most common cause of vision loss
causes of amblyopia
strabismus
cataracts/corneal surgery
anisometropia (differences in the refractive index)
amblyopia treatment
patch/atropine eyedrops (punish good eye)
-gain in amblyopic eye in expense of fellow eye
-little/no improvement in binocular vision
-poor compliance & varied outcome
-only effective in early childhood
temporary monocular deprivation in cats
amblyopia
deficits in binocular vision is restored
10 days of dark exposure recovers eye depression in cats and fluoxetine (prozac) SSRI antidepressant restores critical period plasticity via reduced inhibition, reopens critical period
synaptic scaling experiment
Turrigiano & Nelson, 2004
TTX/CNQX then wash - hyperexcitation
bicuculline then wash - little innervation
potentiation follows depression - requires NMDAR
Bienenstock, Cooper & Munro (BCM) theory of synaptic plasticity
reduced cortical activity = reduced LTD and increased LTP
activity dependence = presynaptic neurons strengthens the synapse only if the postsynaptic neuron is activate (vice versa)
